Neurophysiological Correlates of Emotion Regulationin Children and Adolescents

Marc D. Lewis1, Connie Lamm1, Sidney J. Segalowitz2, Jim Stieben3,and Philip David Zelazo1

Abstract

& Psychologists consider emotion regulation a critical devel-opmental acquisition. Yet, there has been very little researchon the neural underpinnings of emotion regulation acrosschildhood and adolescence. We selected two ERP compo-nents associated with inhibitory control—the frontal N2 andfrontal P3. We recorded these components before, during, andafter a negative emotion induction, and compared their am-plitude, latency, and source localization over age. Fifty-eightchildren 5–16 years of age engaged in a simple go/no-go pro-cedure in which points for successful performance earneda valued prize. The temporary loss of all points triggerednegative emotions, as confirmed by self-report scales. Boththe frontal N2 and frontal P3 decreased in amplitude and la-tency with age, consistent with the hypothesis of increasingcortical efficiency. Amplitudes were also greater following

the emotion induction, only for adolescents for the N2 butacross the age span for the frontal P3, suggesting different butoverlapping profiles of emotion-related control mechanisms.No-go N2 amplitudes were greater than go N2 amplitudesfollowing the emotion induction at all ages, suggesting aconsistent effect of negative emotion on mechanisms of re-sponse inhibition. No-go P3 amplitudes were also greaterthan go P3 amplitudes and they decreased with age, whereasgo P3 amplitudes remained low. Finally, source modeling in-dicated a developmental decline in central-posterior midlineactivity paralleled by increasing activity in frontal midline re-gions suggestive of the anterior cingulate cortex. Negativeemotion induction corresponded with an additional right ven-tral prefrontal or temporal generator beginning in middlechildhood. &

INTRODUCTION

One of the most important tasks of childhood is learningto regulate the impulses that accompany negative emo-tions. This capacity is referred to as emotion regulation,a suite of controls that permit adaptive functioning inthe presence of emotions such as anxiety, anger, shame,distress, and even intense excitement. Under the rubricof emotion regulation, developmental psychologistshave studied normative advances in children’s abilitiesto inhibit emotional impulses, modulate emotionalbehavior, maintain engagement with important fea-tures of the world, and disengage from features thatare emotionally distressing (Posner & Rothbart, 1998;Derryberry & Rothbart, 1997; Thompson, 1994). More-over, individual differences in emotion regulation havebeen found to predict social competence and person-ality development (e.g., Kochanska, Murray, & Harlan,2000). Despite the importance of emotion regulationfor normal development, very little is known aboutits neural underpinnings over the first two decadesof life. Therefore, we looked at cortical activities medi-ating response inhibition—a key aspect of emotion

regulation—during a task that elicited negative emo-tions. Specifically, we measured event-related potentials(ERPs) associated with inhibitory control across a broadage range and tested for differences in their amplitude,latency, and source localization with age and emotioncondition.

Although there has been almost no research examin-ing the neurocognitive correlates of children’s emotionregulation, adults are thought to regulate their emotionsthrough attentional controls mediated by the prefrontalcortex (PFC) and related paralimbic structures such asthe anterior cingulate cortex (ACC) (Bishop, Duncan,Brett, & Lawrence, 2004; Ochsner et al., 2004; Langeet al., 2003; Wong & Root, 2003; Beauregard, Levesque,& Bourgouin, 2001; O’Doherty, Kringelbach, Rolls,Hornak, & Andrews, 2001; Simpson, Drevets, Snyder,Gusnard, & Raichle, 2001; Davidson & Irwin, 1999;Bechara, Damasio, Tranel, & Damasio, 1997). Moreover,neuroscientists have begun to study developmental dif-ferences in these attentional controls, with particularemphasis on response inhibition. Despite some evi-dence for posterior cortical involvement for youngerchildren (Bunge, Dudukovic, Thomason, Vaidya, &Gabrieli, 2002), attentional control is generally asso-ciated with prefrontal activities at all ages. Moreover,1University of Toronto, 2Brock University, 3York University

D 2006 Massachusetts Institute of Technology Journal of Cognitive Neuroscience 18:3, pp. 430–443

several studies indicate less prefrontal activation aschildren mature. Neuroimaging research shows lessprefrontal activation in adults than in children (Durstonet al., 2002; Casey et al., 1997) and adolescents (Lunaet al., 2000) in tasks requiring inhibition or directedattention. This reduction may be explained by increasingneural efficiency, such that less neural processing isnecessary to achieve successful performance later indevelopment (Casey, Giedd, & Thomas, 2000). It mayalso indicate that synaptic pruning and myelinationunderlie increasing cognitive integration over develop-ment (Casey et al., 2000; Luna et al., 2000). ERP findingsare partly consistent with this picture in that a numberof studies point to decreased frontal ERP amplitudeswith age. However, before reviewing these findings, it isnecessary to (1) specify which ERP components areassociated with frontally mediated mechanisms of re-sponse inhibition and (2) determine how they might berelated to emotion.

Only two ERP components have been consistentlylinked with response inhibition. The first is a frontal N2,observed about 200–400 msec poststimulus at medial-frontal sites. The frontal N2 is generally reported onsuccessful no-go trials (Falkenstein, Hoormann, &Hohnsbein, 1999; Eimer, 1993; Jodo & Kayama, 1992)and is thus referred to as the ‘‘inhibitory’’ or no-goN2. However, robust N2s have been found on gotrials as well (e.g., Davis, Bruce, Snyder, & Nelson,2003; Nieuwenhuis, Yeung, Van den Wildenberg, &Ridderinkhof, 2003). Although the frontal N2 is usuallyinterpreted in terms of response inhibition or anticipa-tory attention, some authors propose that it marks themonitoring of conflict between competing responsesor task representations (Nieuwenhuis et al., 2003;Botvinick, Braver, Barch, Carter, & Cohen, 2001). Thus,the N2 might be considered an ‘‘evaluative negativity,’’whose psychological functions include effortful atten-tion or action monitoring (Tucker, Luu, Desmond, et al.,2003). The second ERP component associated withresponse inhibition is the frontal (or ‘‘inhibitory’’) P3,also generally reported on successful no-go trials. Thiscomponent is observed at medial-frontal sites in adults,approximately 300–500 msec poststimulus, somewhatlater than the P3 observed at parietal sites (e.g., Bruin& Wijers, 2002; Bokura, Yamaguchi, & Kobayashi, 2001;Strik, Fallgatter, Brandeis, & Pascual-Marqui, 1998; Kopp,Mattler, Goertz, & Rist, 1996). The role of the frontalP3 in response inhibition has been the subject of somediscussion. Falkenstein et al. (1999) interpret it as theclosing of an inhibition window whose onset is markedby the earlier N2 component. Alternatively, Bokuraet al. (2001) suggest that larger frontal P3 amplitudescorrespond with lower-probability stimuli, similar toNieuwenhuis et al.’s (2003) interpretation of the fron-tal N2.

Because both of these ERPs have been linked with theinhibition of prepotent or impulsive responses, we

assumed that they would tap cognitive processes in-volved in emotion regulation. Is there evidence tosuggest a connection with emotion? Indeed, negativeemotional evaluations have been found to predict higher-amplitude medial-frontal N2s (Tucker, Luu, Desmond,et al., 2003), and a feedback-related negativity, similar tothe N2 in topography and morphology, was enhancedby negative evaluations (Luu, Tucker, Derryberry, Reed,& Poulsen, 2003). Amplitudes of both the feedback-related N2 (Tucker, Luu, Frishkoff, et al., 2003) andthe frontal P3 (Deldin, Keller, Gergen, & Miller, 2001)have also been found to correlate with depression.Moreover, Nelson and Nugent (1990) found a fronto-central negativity similar to the N2 in young children,showing larger amplitudes to angry than happy faces,hypothetically indexing attentional processes related toemotional content. The cortical generators associatedwith medial-frontal ERPs (including the error-relatednegativity) also suggest links with emotion. Sourcemodeling of these components reveals a key generatorin the region of the ACC, a structure thought to inte-grate cognition and emotion (e.g., Bekker, Kenemans, &Verbaten, 2005; Luu et al., 2003; Nieuwenhuis et al.,2003; Tucker, Luu, Desmond, et al., 2003; van Veen &Carter, 2002; Bokura et al., 2001; Fallgatter, Mueller, &Strik, 1999; Dehaene, Posner, & Tucker, 1994). This isconsistent with the idea that emotion regulation iscarried out by the cognitive processes tapped by thesecomponents. Similarly, the region of the orbitofrontalcortex (OFC), another area integrating attention andemotion, has been identified as a generator of the N2and frontal P3 in several studies (Bokura et al., 2001;Pliszka, Liotti, & Woldorff, 2000). More important, bothchildren and adults show increased fMRI activation inboth the ACC and OFC during response inhibition(Casey et al., 1997). Taken together, these findingssuggest that ERPs such as the N2 and frontal P3 maytap inhibitory control in response to negative emotionalstates, as mediated by prefrontal regions including theACC and possibly the OFC.

Having selected a pair of ERPs that tap responseinhibition and having addressed their potential role inemotion regulation, we can now ask what is knownabout the development of these ERPs. Developmen-tal research with go/no-go tasks has consistently showna decrease in N2 amplitude (and latency) with age( Johnstone, Pleffer, Barry, Clarke, & Smith, 2005; Daviset al., 2003; Jonkman, Lansbergen, & Stauder, 2003).This profile is to be expected because it matches fMRIevidence for decreasing prefrontal activity with age inattentional control tasks. However, inhibitory P3 resultsare mixed: 6-year-olds showed higher-amplitude P3sthan adults on no-go trials as well as more difficult gotrials (Davis et al., 2003), but Jonkman et al. (2003)report the absence of a no-go P3 for children, andJohnstone et al. (2005) report smaller anterior P3s forchildren than adults. These discrepancies are difficult to

Lewis et al. 431

reconcile because all tasks assessed inhibitory controlusing a go/no-go procedure.

The mixed findings reviewed here suggest the needfor systematic developmental research into ERPs tappinginhibitory control. However, a number of design short-comings should be addressed by this research. First, thetasks utilized for developmental studies are generallyboring. Whereas adults are able to attend to boring tasksfor long periods of time in the service of long-term re-wards (e.g., participant payments), children are notori-ously unable to do so. Hence, age differences in theneural correlates of executive processes are probably con-flated with age differences in motivational proclivities,endurance, and fatigue effects, and these factors maycontribute greatly to discrepancies among studies. Sec-ond, developmental studies usually compare one agegroup with adults (but see Davies, Segalowitz, & Gavin,2004, for an exception). Different studies select differentage groups for this comparison, each using differenttasks. Consequently, their findings are difficult to inte-grate into a coherent picture of development. In orderto map out a developmental profile in a parameter suchas inhibitory control, it is necessary to administer similaror commensurate tasks to children of many differentages. Finally, to date, no ERP studies of children haveused source analysis techniques, probably due to the highdegree of variability in children’s waveforms and the con-sequent ‘‘smearing’’ of the grand-averaged data. This hasprecluded developmental comparisons of the cortical re-gions likely to be associated with the cognitive processestapped by ERP measures—a critical next step for devel-opmental neuroscience (Segalowitz & Davies, 2004).

Our design attempted to deal with each of these kindsof problems. First, the task itself was designed to beengaging and, in fact, emotionally compelling to chil-dren of all ages by highlighting the gain and loss ofpoints that could be cashed in for a valued prize. Thespeed of stimulus presentation was also adjusted dy-namically, in response to participants’ performance ac-curacy, to maintain an error rate of approximately 50%(see Garavan, Ross, & Stein, 1999). Thus, there was nochance that the task was too slow for some participantsor too fast for others. Second, rather than compare oneage group with adults, we looked at children’s ERPsacross a broad span of development, from 5 to 16 years.This permitted us to map out a reasonably fine-grainedprofile of developmental change. Commensurability wasensured by the dynamic adjustment procedure, whichproduced equivalent error rates across the age span.Finally, we reduced the variability in our data by select-ing subjects (in each age group) with well-defined ERPcomponents prior to source modeling. This allowed usto compare source models across age and hence to drawtentative conclusions about developmental differencesin regions of activation.

Our paradigm integrated a go/no-go task with anemotion-induction procedure. Children were required

to click a button each time a letter appeared but torefrain from clicking when the same letter showed uptwice in succession. Every 20 trials, an on-screen windowdisplayed the points they had earned for correct re-sponses. In order to insure motivation, the childrenwere shown desirable toys or gift certificates (dependingon age) prior to the procedure, and they were remindedseveral times that they needed to earn a high number ofpoints to receive one of these rewards. The task wasdivided into three blocks, and points rose for all childrenduring Block A. However, points began to drop precip-itously in Block B and ended up back at zero. This blockwas expected to induce negative emotions such asanxiety, frustration or anger, and distress. Finally, pointsrose again during Block C so that a prize could beawarded after all, yet we expected that the negativeemotions induced in Block B would carry over intoBlock C for many children. Approximately one-third ofall trials were no-go trials. This was to ensure anadequate number of successful no-go trials for averagingthe N2 and frontal P3 despite a limited number of trialsper block to minimize fatigue and boredom.

We expected amplitudes and latencies for correctno-go trials to diminish with age for both ERP compo-nents, consistent with ERP and fMRI findings of age-related decreases in activation suggestive of increasingcortical efficiency. We also predicted higher amplitudesgenerated by the emotion induction in Block B andpossibly lasting through Block C, reflecting increasedefforts at response inhibition in the presence of nega-tive emotion. Finally, we expected source models ofthe stimulus-locked waveform to reveal age differencesin cortical generators, with older children showing re-gions of activation more similar to those reported inadults.

METHODS

Participants

Participants were 58 English-speaking children ages 5–16(28 boys), with normal or corrected-to-normal vision,and free of any psychiatric diagnoses. This age span wassubdivided into six periods of 2 years each (see Table 1).Participants were recruited through a local newspaperand paid CDN $40.00 plus a toy or gift certificate fortheir participation. Ethical approval of the project wasobtained from the University of Toronto and the Hos-pital for Sick Children in Toronto.

Procedure

Children were accompanied to the laboratory by aparent. Following a brief introduction to the testingenvironment, electrode sensor nets, and recording sys-tem, parental consent and child assent were obtained.Children were informed that they would receive a prize

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for playing the computer game and were shown two toybins. One of the bins contained small, undesirable toyssuch as small plastic cars, whereas the second bin con-tained more desirable, age-appropriate toys such as largeaction figures, arts and crafts sets, large stuffed animals,games, and $10.00 gift certificates from a local musicstore for the older participants. The children were in-formed that with successful performance (accumulationof points) in the game they would have their choice ofrewards, but that less successful performance would limittheir choice to the less desirable toy bin. The childrenwere asked to choose a toy (or gift certificate) they wouldlike to earn. The electrode sensor net was then appliedand the child was seated in front of a computer moni-tor, with the distance and alignment to the monitor con-trolled by use of a chin rest. Children were instructed tomake responses in the game by clicking a button ona response pad with the index finger of their dominanthand (writing hand). Children were given a practice blockof 30 trails to ensure proficiency with the task, withthe opportunity to repeat the practice block if needed.Children and parents were fully debriefed about the pur-pose of the study after two more longitudinal waves (tobe described in a forthcoming report).

Task

The emotion-induction go/no-go task used in the pres-ent study was partly adapted from a task developed byGaravan et al. (1999) and presented using E-Primesoftware (Psychological Software Tools, Pittsburgh, PA).In standard go/no-go paradigms, participants are re-quired to press a button as fast as possible given aparticular category of stimuli (the go condition) andwithhold responding given another category of stimuli(the no-go condition). Our participants were instructedto click the button for each letter presented but to avoidclicking when a letter was repeated a second time insuccession. Different pairs of similarly shaped letterswere used for each block (Block A: x, y; Block B: o, p;

Block C: u, d) to enhance novelty without modifying thelevel of difficulty and to facilitate guided recall duringa self-report scale administered to a subset of partici-pants. The no-go error rate for the task was maintainedat 50 ± 10% by adjusting the stimulus duration (and thusthe intertrial interval) dynamically. Stimulus duration wasincreased with each error made on a no-go trial anddecreased with each correct response (on no-go trialsthat followed correct go trials only). This was intendedto provide the same level of challenge for all partici-pants at all ages and to obtain a sufficient number ofcorrect no-go trials for ERP averaging. Error feedback wasprovided by a red bar in the middle of the screen fol-lowing incorrect responses, omitted responses, and lateresponses.

Children were reminded at the beginning of the taskand the outset of each block that a high number ofpoints was needed to win the ‘‘big prize’’ they hadchosen. Every 20 trials, their accumulated points weredisplayed in red in a window on the screen. Points wereadded for correct no-go responses and deducted forresponse errors on both go and no-go trials. Threeblocks of trials were presented: A, B, and C. Blocks Aand C were structurally identical, each consisting of 200trials (including 66 no-go trials in pseudorandom se-quence). Block B consisted of 150 trials (40 no-go trials),to limit the duration of children’s distress during thepoints-loss condition. In Block A, children saw theirpoints steadily increase, usually to over 1000. However,changes in the point-adjustment algorithm caused themto lose all their points by the end of Block B. With areturn to the more generous algorithm, children thenregained their points in Block C to win the desirableprize. The loss of points in Block B was intended toinduce emotions of anxiety, anger, and/or distress at thepossible loss of the prize.

Manipulation Check

This emotion-induction scheme was tested with a sub-jective rating scale administered in a second ERP ses-sion. This session was conducted with 19 children in the8–12-year-old range, approximately 12 weeks after theinitial testing. At the end of the task, children rated eachof the three blocks (using the different letter pairs asreminders) on a 10-point Likert scale for five emotions:‘‘upset,’’ ‘‘mad,’’ ‘‘nervous,’’ ‘‘satisfied,’’ and ‘‘excited.’’Cards showing animated emotion faces of differentintensities were used to aid recall.

EEG Data Collection and Analysis

EEG was recorded using a 128-channel Geodesic SensorNet (Tucker, 1993) and sampled at 250 Hz, using EGIsoftware (EGI, Eugene, OR). Impedances for all EEGchannels were kept below 50 k�. All channels werereferenced to Cz (channel 129) during recording. Eye

Table 1. Number of Participants in Each Age GroupPartitioned by Sex

Sex

Age Group (yrs) Male Female Total

5–6 1 2 3

7–8 6 4 10

9–10 7 4 11

11–12 7 7 14

13–14 3 7 10

15–16 4 6 10

Total 28 30 58

Lewis et al. 433

blink and eye movement artifacts (70 AV threshold), sig-nals exceeding 200 AV, and fast transits exceeding 100 AVwere edited out during the averaging. The EEG wasthen rereferenced against an average reference (Tucker,Liotti, Potts, Russell, & Posner, 1993; Bertrand, Perrin, &Pernier, 1985). Data were filtered using an FIR band-passfilter with a low-pass frequency of 30 Hz and a high-passfrequency of 1 Hz. Stimulus-locked data were segmentedinto epochs from 400 msec before to 1000 msec afterstimulus onset. Trials with response times shorter than200 msec or longer than 1000 msec were removed, asthey were assumed to reflect nondeliberate behavior.Also, correct no-go trials that did not have a correct gotrial preceding and following them were removed be-cause they most likely reflected attentional lapses orchronic nonresponding. Final trial count means werecalculated by block (22.86 for Block A, 11.64 for Block B,and 25.19 for Block C) and by age (18.23, 18.88, 18.71,23.27, and 20.27 from youngest to oldest). Because therewere fewer no-go trials in Block B, we reran tests foramplitude differences by block for both the N2 and P3,with trial count as a covariate, and found very littlechange in the results. A baseline correction factor wascalculated over 400 msec preceding the stimulus.

ERP components were scored using the followingcriteria: The N2 was coded as the largest negative deflec-tion after the N1 with a medial-frontocentral topographyand with a latency between 200 and 500 msec poststim-ulus. The frontal P3 was coded as the largest positivedeflection after the N2 with a medial-frontocentral to-pography, and with a latency between 250 and 1000 msecpoststimulus. Scoring was carried out by a coder blindto the ages of the participants. The latency for eachcomponent was recorded as the latency to the peakidentified in the amplitude analysis.

Source Analysis

In order to estimate the cortical generators of the stimulus-locked waveform, temporal–spatial dipole source modelingwas performed on non-baseline-corrected, grand-averageddata using brain electrical source analysis (BESA; Berg& Scherg, 1994). Equivalent dipole models were derivedusing a spherical head model with an isotropic realistichead approximation factor of 20. Dipoles were con-secutively fitted along the stimulus-locked waveform av-eraged over correct no-go trials, starting approximately50 msec after the stimulus onset. A final solution was con-sidered adequate when the residual variance was lessthan 10% (Berg & Scherg, 1994).

RESULTS

In order to identify a fine-grained developmental profilein behavioral and neurophysiological analyses, we sub-divided the age span into six periods of 2 years each

(ages 5–6, 7–8, 9–10, 11–12, 13–14, 15–16). The youn-gest group was dropped because it contained only threemembers, but all other groups contained at least 10, asshown in Table 1. Furthermore, because previous re-search suggests that boys and girls may differ in thetiming of neural development, we entered sex as acovariate for all analyses (both behavioral and ERP) thatincluded age as a factor. Sex effects were observed for afew analyses; however, because none were predictedand these effects were not systematic, we do not reportthem here.

Behavioral Analyses

Accuracy Results

Because perseverative responding leads to high accu-racy on go trials and low accuracy on no-go trials, andchronic nonresponding leads to high accuracy on no-gotrials and low accuracy on go trials, we needed anaccuracy measure that combined go and no-go accuracyscores in some reasonable fashion. We chose the sim-plest measure possible: an average of go and no-goaccuracy scores, computed by averaging the means foreach trial type. Low scores on either go or no-go trialswould pull down the mean, yielding a lower overallscore. Using this measure, we found a main effect ofage, with older children showing higher accuracythan younger children, F(4,49) = 8.67, p < .001 (seeFigure 1). Planned contrasts revealed lower accuraciesfor the 7–8- and 9–10-year-olds than for all older

Figure 1. Age differences in accuracy by block. Accuracy wascomputed by averaging the means for go and no-go trials.

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groups ( p values ranging between .03 and < .001), andlower accuracies for the 11–12- than the 13–14-year-olds( p = .02). As would be expected, a quadratic blockeffect revealed lowest accuracy scores for Block B(the emotion-induction block), F(1,49) = 33.85, p <.001. Thus, heightened challenge or negative emotionseemed to compromise performance. A quadratic blockby age interaction revealed lower accuracy for youngerchildren than older children in Block B, indicating lessinterference with increasing age, F(4,49) = 4.42, p =.004. This is reflected by the narrowing gap over agebetween Blocks A and B in Figure 1.

Response Time Results

Both go and no-go response times were measuredfrom stimulus onset. A main effect of age was found,with older children showing faster response times forboth the go condition, F(4,49) = 17.25, p < .001, andthe no-go condition (error trials only), F(4,49) = 11.70,p < .001. Planned contrasts revealed slower responsetimes for the 7–8-year-olds than all other age groups,for both go and no-go conditions ( p < .001), slowerresponse times for the 9–10-year-olds than the 13–14-and 15–16-year-olds for both conditions ( p valuesranging between .03 and .003), and slower responsetimes for the 11–12-year-olds than the 13–14- and15–16-year-olds for the go condition ( p = .03) butonly the 13–14-year-olds for the no-go condition ( p =.02). A 2 (condition) � 3 (block) � 5 (age group)ANOVA, with repeated measures for condition andblock, revealed a main effect of condition, indicatingthat error (no-go) response times were faster than cor-rect (go) response times across age, F(1,49) = 15.74,

p < .001. Thus, error trials were associated with morerapid responding, probably indicating greater impulsiv-ity. Figure 2 reveals the linear decrease in response timewith age for both conditions, as well as more rapid re-sponse times for the no-go trials overall.

ERP Analyses

We began the ERP analyses by comparing amplitudesacross age at three frontocentral-medial sites (11, 6, and129, corresponding to Fz, FCz, and Cz, respectively) andselecting the site that showed the greatest mean agedifferences for each component. This reduced the over-all number of comparisons and highlighted the devel-opmental differences that were the focus of this study.Based on this comparison, frontal P3 analyses wereconducted at Fz and N2 analyses were conducted atFCz. Figure 3 presents the grand-averaged waveforms ofthe N2 and frontal P3 components (at their respectiveelectrode sites). As mentioned earlier, grand-averagedwaveforms can be smeared due to high variability acrossindividual subjects’ waveforms, and this is evident forthe children in our sample. Furthermore, the amount of

Figure 2. Age differences in response times for go and no-goconditions, collapsing across blocks.

Figure 3. Age and block differences in stimulus-locked, grand-averagedwaveforms (for no-go trials) for the N2, at site FCz (top), and the

frontal P3, at site Fz (bottom).

Lewis et al. 435

variability can differ greatly from one component toanother, as reflected by standard deviations in latency.The mean SDs for the latencies of the N2 and frontalP3, collapsing across blocks and ages, were 45.56 and183.33 msec, respectively. Thus, latencies were relativelyhomogeneous for the N2 but heterogeneous for theP3, as reflected in Figure 3.

Figure 3 (top) reveals distinct and sequential age dif-ferences in amplitudes and latencies for the N2, espe-cially for Block A. Age differences are evident but muchless distinct for the P3, apparently due to high variabilityin latencies. Because the difference between baselineactivation (Block A) and activation during the emotioninduction (Block B) is of primary interest here, wave-forms for Block C are not presented. The followingstatistical analyses examine age and block differencesin detail. For each ERP component, we first presentage and block results for the no-go trials only, in orderto test the hypothesized effects of age and emotioninduction on inhibitory control. We then test for dif-ferences between go and no-go trials, to better charac-terize these findings.

Frontal N2 Results

All N2 results are based on the correct no-go ERP un-less otherwise specified. A 5 (age group) � 3 (block)repeated-measures ANOVA (with gender as a covariate)revealed a main effect of age for N2 amplitudes, withsmaller amplitudes for older children, as predicted,F(4,48) = 2.66, p = .04. Planned contrasts showedsignificantly greater amplitudes for the 7–8- and 9–

10-year-olds than the 15–16-year-olds ( p = .003 and .02,respectively). Contrasts also revealed smaller values forthe 15–16-year-olds than the 11–12 and 13–14-year-oldsat the level of a trend ( p = .08). As can be seenin Figure 4, the developmental profile for the N2 isstrikingly linear, at least for the A block. However, theemotion-induction (B) block can be seen to increaseamplitudes for the oldest two age groups. Indeed, con-trasts revealed greater amplitudes for Blocks B andC than Block A for the 15–16-year-olds ( p = .04), andgreater values for Block C than A for the 13–14-year-olds( p = .05). Thus, older children appeared more sen-sitive to the emotion induction or its aftermath. Anadditional age � block analysis of N2 latencies (withidentical syntax) also revealed the predicted main effectof age, with older children showing faster latencies,F(4,48) = 10.75, p < .001. Planned contrasts revealedlonger latencies for the 7–8-year-olds than all otherage groups ( p values ranging between .03 and < .001),and longer latencies for the 9–10 and 11–12-year-oldsthan the 13–14- and 15–16-year-olds ( p < .005). Fig-ure 5 indicates a roughly linear decrease in N2 latencieswith age.

To determine if the no-go N2 differed from the goN2 in amplitude or latency, two 2 (condition) � 5 (agegroup) � 3 (block) ANOVAs were conducted. Consist-ent with the literature, N2 amplitudes were greaterfor no-go trials, F(1,49) = 6.25, p = .02, and latencieswere faster for no-go trials as well, F(1,49) = 13.22,p = .001. We also found a linear condition by blockinteraction for amplitudes, F(1,49) = 5.43, p = .02.

Figure 4. Age differences in N2 amplitudes (at site FCz) by block.

Figure 5. Age differences in N2 latencies (at FCz) by block.

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Bonferroni-corrected contrasts revealed that no-goamplitudes were only greater than go amplitudes forBlocks B ( p = .04) and C ( p = .008), suggesting animpact of the emotion induction on processes of in-hibitory control. There was no interaction with age.Children of all ages thus showed higher amplitudesand faster latencies when they had to withhold theirresponses, consistent with the idea that the N2 tapsinhibitory control across development.

Frontal P3 Results

All frontal P3 results are based on the correct no-go ERPunless otherwise specified. A 5 (age group) � 3 (block)repeated-measures ANOVA (with gender as a covariate)revealed a main effect of age for P3 amplitudes, witholder children showing smaller values than youngerchildren, as predicted, F(4,48) = 4.75, p = .003. Plannedcontrasts showed greater amplitudes for the 7–8-year-olds than the 11–12, 13–14, and 15–16-year-olds ( p val-ues ranging between .009 and < .001), and greatervalues for the 9–10-year-olds than the 11–12 and13–14-year-olds ( p = .05). As can be seen in Figure 6,amplitudes declined relatively steeply at first but thenleveled out in the older age range. In addition, aspredicted, a quadratic block effect indicated an increasein P3 amplitudes in Block B, F(1, 48) = 8.59, p = .005.Planned contrasts revealed greater amplitudes in BlockB than Block A for the 11–12-year-olds ( p = .01), andgreater values in Block B than Block C for the 7–8-,9–10, and 11–12-year-olds ( p values range between .04

and .001). These results indicate that the emotioninduction increased cortical activation tapped by theP3 across most of the age range. Frontal P3s not onlygrew smaller with development but they appearedearlier too, as shown by a main effect of age on latencies,F(4,48) = 5.92, p = .001, in an additional age � blockANOVA. Figure 7 indicates a gradual decrease in laten-cies over the first four age points, followed by a rapiddrop for the oldest group. Indeed, contrasts revealedshorter latencies for the 15–16-year-olds than all otherage groups ( p < .002).

To determine if the no-go P3 differed from the go P3in amplitude or latency, two 2 (condition) � 5 (agegroup) � 3 (block) ANOVAs were conducted. Maineffects of condition were found for both amplitudesand latencies: No-go amplitudes were greater than goamplitudes, F(1,49) = 116.09, p < .001, but no-golatencies were longer than go latencies, F(1,49) =128.69, p < .001. Thus, frontal P3s were more robust,but later, on trials requiring response inhibition. Aquadratic condition by block interaction effect was alsorevealed, indicating greatest no-go amplitudes, but notgo amplitudes, for Block B, F(1,49) = 11.61, p = .001.Moreover, Bonferroni-corrected contrasts showed great-er amplitudes for no-go P3s than go P3s for all threeblocks ( p < .001), even though Block B was the mostaugmented. Finally, a linear condition by age interac-tion effect revealed that no-go P3 amplitudes decreasedwith age, whereas go P3 amplitudes did not, F(4,49) =8.05, p < .001. This differentiation is clearly shown inFigure 8, which collapses across blocks for ease ofviewing. Bonferroni-corrected contrasts revealed greaterFigure 6. Age differences in frontal P3 amplitudes (at site Fz) by block.

Figure 7. Age differences in frontal P3 latencies (at site Fz) by block.

Lewis et al. 437

amplitudes for the no-go condition than the go con-dition for all age groups ( p values range from .02 to< .001), indicating that no-go amplitudes decreased withage but never to the level of go amplitudes.

Associations with Stimulus Duration

Our task relied on the dynamic adjustment of stimulusduration to equalize performance difficulty across par-ticipants and across age. Although this innovation wasuseful, it introduced associations between stimulus du-ration and ERP differences that required further explo-ration. We first correlated stimulus duration with (theabsolute value of ) ERP amplitudes. Correlations werepositive (for both components) for all three blocks,meaning that children with longer stimulus durationsshowed greater amplitudes. This was not surprising,because both probably tapped greater effort or poorercompetency. Because this association implied sharedvariance among age, competency, stimulus duration,and ERP amplitudes, we next redid the age analyses withstimulus duration as a covariate. When covariance withstimulus duration was removed, the effect of age onamplitude was reduced. For the P3, the main effect ofage remained significant, F (4,46) = 2.70, p < .05; forthe N2, only the contrast for Block A remained signifi-cant ( p < .05). We also covaried stimulus duration outof the latency analyses and found that the effect of ageon latency remained unchanged. Further work will berequired to disentangle the effects of age and stimulusduration, both of which may tap some of the sameunderlying factors.

Mean amplitude was greatest in Block B (for the P3component), whereas mean stimulus duration was

shortest. However, in contrast, amplitude and stimulusduration were positively correlated, as just noted, andtheir correlation was stronger in Block B (r = .46, p <.001) than in Blocks A and C (rs = .27 and .17). This maysuggest that longer-than-average stimulus durations inBlock B reflected poorer performance specifically relat-ed to the emotion induction. Greater efforts (by somechildren) to regulate behavior in the presence of nega-tive emotion may have corresponded with higher errorrates, thus increasing stimulus duration for those mostaffected by the emotion induction. Indeed, enteringstimulus duration as a covariate reduced the quadraticeffect of block on P3 amplitudes below significance. Wesuggest that this procedure removed much of the effectof the emotion induction itself.

Emotion Scale Results

A subjective rating scale was used to assess the emotion-induction feature of the task. This scale was admin-istered to a subset of 19 8–12-year-old participantsduring a second administration of the task. The scalerequired children to rate the intensity of satisfaction,excitement, nervousness, ‘‘upset,’’ and ‘‘mad’’ felt dur-ing each block of the task. Analysis of the data revealed asignificant quadratic effect for block for all five descrip-tors. Block B showed the highest mean endorsementsfor mad, F(1,18) = 15.17, p = .001, upset, F(1,18) =13.60, p = .002, and nervous, F(1,18) = 7.72, p = .01.Block B also received the lowest mean endorsements forsatisfaction, F(1,18) = 46.19, p < .001, and excitement,F(1,18) = 72.51, p < .001. The high negative and lowpositive endorsements for Block B help ascertain thatmost children felt frustration and/or anxiety when theirpoints were rapidly deducted.

Although we did not plan to use these scores as areliable index of individual differences in emotion in-duction, it seemed useful to correlate self-report scoreswith the amount of change in P3 amplitude from Block Ato B for this sample (there were no amplitude effects forthe N2 in this age range), to determine whether re-ported negative emotion covaried with the degree ofamplitude change. The three negative emotion scaleswere averaged, and this value was normalized through alog transformation. This composite score was thencorrelated with the difference score obtained by sub-tracting Block A amplitudes from Block B amplitudes.With all children included, there was a weak positivecorrelation between negative emotion scores and am-plitude increases, r = .27, p = ns. However, when weredid the analysis including only children 10 and older,who were presumably more precise in their self-report,this correlation was strengthened, r = .54, one-tailedp = .05. These results help support the argument thatincreasing Block B amplitudes reflected the impact ofnegative emotion.

Figure 8. Age differences in frontal P3 amplitudes for go versus

no-go conditions (at site Fz), collapsing across blocks.

438 Journal of Cognitive Neuroscience Volume 18, Number 3

Source Analysis

Source analysis was conducted to determine if theneural generators underlying children’s ERPs variedacross age and if the location or activation of thesegenerators changed with the emotion induction. Threesteps were undertaken to clean up the variability thatcan hamper source modeling of child ERP data. First,because N2s showed the least variability in latency, weselected the peak of the N2 component for presenta-tion. Second, to obtain a pool of sufficient size foraveraging at several ages, we redivided our sample intothree groups of 4 years each. Finally, to clean upamplitude variability, we selected half the children fromeach of these age groups: those with the highest N2amplitudes (at site FCz). Though this selection no doubtbiased the source models, it did so in a consistentfashion across age, thus allowing meaningful develop-mental comparisons. Stimulus-locked grand averageswere generated for each age group using only thepreselected children.

As can be seen in Figure 9 (top), peak N2 activity forthe 5–8-year-olds was characterized by a strong centro-medial source in the region of the mid- or posteriorcingulate cortex for Blocks A and B. As seen in Figure 9(middle), the 9–12-year-olds showed the same centro-medial source, suggesting mid- or posterior cingulateactivation, but it appeared weaker for both blocks. Astrong right ventral source emerged in Block B as well,suggestive of activation in the OFC or temporal pole. Asseen in Figure 9 (bottom), the 13–16-year-olds showedthe centromedial source only in Block B, along with aweaker version of the right ventral source shown by the9–12-year-olds. These children also showed a medial-frontal source in the region of the dorsal ACC, ofequivalent strength and appropriate orientation in bothBlocks A and B. Inspection of the source models acrossage suggests a developmental decline in the activationof a mid- or posterior cingulate generator roughlyparalleling increased activation of an anterior cingulategenerator, indicating a general frontalization of activa-tion with age. Block B differed from Block A only in theappearance of a right OFC or inferior temporal sourcefor the middle and older age groups. Examination ofthe topographic plots presented in Figure 9 highlightsthe decrease in scalp activation with age. Furthermore,an increase in activation from Block A to B is onlyevident for the oldest group, consistent with the statis-tical analyses.

DISCUSSION

Accuracy improved and response time decreased withage, consistent with other studies comparing childrenwith adults (e.g., Jonkman et al., 2003). Moreover,response time was fastest and accuracy was lowest onBlock B, the emotion-induction block, at all ages, sug-

gesting more impulsive responding when the emotionalstakes were raised. Children probably became more‘‘desperate’’ when they found their points droppingrapidly and they began clicking more indiscriminatelyas well as more quickly. The increase in errors producedby this response style would have slowed stimuluspresentation, given the dynamic adjustment algorithm.However, points would continue to drop (in Block B)regardless of children’s efforts, and impulsivity mightpersist or recur repeatedly as a consequence of ongoingfrustration. Interestingly, the tendency toward poorerB-block accuracy diminished with age. Older childrenmay have been better able to inhibit impulsive clickingdespite frustration or anxiety, or they could have beenless upset, but this too might be considered a conse-quence of improved regulatory abilities. This trendcaptures one of the most important, if obvious, gainsof growing up: a capability for effortful self-controldespite continuing indications of failure. Finally, morerapid responding on no-go trials at all ages indicates thatimpulsivity may have been partly responsible for errors,as would be expected in a speeded go/no-go task.

N2 amplitudes and latencies decreased with age, aspredicted. These findings are consistent with the hy-pothesis that cortical mechanisms of inhibitory controlbecome more efficient with development (e.g., Caseyet al., 2000). Moreover, the reductions in amplitude andlatency showed a remarkably linear profile across thefive age points, at least for Block A (prior to the emotioninduction). This may suggest that developmental im-provement in the efficiency of cortical attentional mech-anisms continues steadily throughout childhood andadolescence without leveling off until at least late ado-lescence. However, N2 amplitudes for Blocks B and Cbranched off this linear trend for children 13–16 years ofage. Higher amplitudes following the emotion inductionsuggest more extensive or more effortful activation ofresponse inhibition mechanisms when anxiety or frus-tration threatened performance. Yet, our prediction ofhigher amplitudes beginning with Block B, arguablytapping emotion regulation, was borne out for the olderchildren only. The age by block interaction effect foraccuracy, indicating that older children’s accuracy dete-riorated less in Block B, may reflect the impact of thisage-related increase in regulatory efforts.

According to this line of reasoning, older childrenregulate their behavior in response to anxiety, frustra-tion, or challenge by ‘‘amping up’’ cortical activities thathave become more efficient with age (consistent withthe suggestion of more effortful processing). However,another overlapping interpretation is that young chil-dren were already regulating their behavior at fullcapacity in Block A. Working to gain points in anunfamiliar game, and wearing an unfamiliar cap on one’shead in the presence of strangers, might not be devoidof anxiety, even when one appears to be ‘‘winning.’’Thus, older children may have been less anxious at

Lewis et al. 439

baseline and hence exerting less than maximal effort. Itis also conceivable that the gain and loss of points wasmore meaningful to the older children, making themmore sensitive to the change in their success rate inBlock B. However, this seems less likely given that

younger children expressed the same concerns, feltemotions, and enthusiasm for the prize.

N2 amplitudes were greater for no-go than go trials, asexpected, but this difference was specific to Blocks Band C and thus presumably related to emotion induc-

Figure 9. BESA equivalent dipole models for three age groups, based on stimulus-locked, grand-averaged, correct no-go waveforms, shownat peak N2 amplitudes for Blocks A and B. Dipole sizes are proportional to activation strength using the same scale across age groups.

440 Journal of Cognitive Neuroscience Volume 18, Number 3

tion. In studies of adults, both go and no-go trialsproduce N2s, but most studies report higher amplitudesfor no-go trials, consistent with the characterization ofthe N2 as inhibitory. Studies of children find mixedresults. For example, Davis et al. (2003) found no differ-ences between go and no-go amplitudes with 6-year-oldchildren, whereas Johnstone et al. (2005) and Overtoomet al. (1998) report greater amplitudes for no-go trials. Itis possible that some emotional highlighting is necessaryfor children, and possibly adults, to increase their atten-tional efforts in the service of inhibition as comparedwith anticipatory evaluation. A task requiring letterdiscrimination might be particularly boring to children,such that an added motivational component was neces-sary to maximize the cortical activities underpinninginhibitory control.

Developmental patterns for the frontal P3 were verysimilar to those for the N2, with both amplitude andlatency diminishing over age, consistent with the hy-pothesis of increasing cortical efficiency. These resultscontradict Johnstone et al.’s (2005) observation of in-creasing amplitudes with age but agree with their find-ings with respect to latency. Given Jonkman et al.’s(2003) finding of no inhibitory P3s in children, onemight conclude that task factors and emotional saliencemake a big difference in the cortical activities tappedby this component. In our data, the relatively steadychange in P3 amplitudes and latencies (across five agepoints) gives us some confidence that the observeddevelopmental decrease is not spurious. We attributethe consistency of our data to the fact that children werehighly engaged, motivated, and concerned with theirperformance at all ages. However, the developmentalprofile of P3 amplitudes appeared to level out in the lasthalf of the age range, whereas the developmental profileof P3 latencies dropped most sharply during these years.These results require replication before we attempt tointerpret them. Children of all ages showed enhancedP3s in the emotion-induction block, consistent with ourpredictions. Thus, cortical activation mediating inhibito-ry control again appeared to be greatest in the presenceof negative emotions, perhaps reflecting the need formore effortful processing. We cannot explain why P3amplitudes corresponding with the emotion inductionincreased at all ages, whereas N2 amplitudes increasedonly for older children. Perhaps, even for youngerchildren experiencing anxiety in Block A, the frontal P3was not yet at its ceiling level.

Frontal P3 amplitudes were greater for no-go than gotrials. However, unlike the N2, this effect was evident inall blocks. This finding is consistent with studies of thefrontal P3 in adults and children (e.g., Johnstone et al.,2005; Fallgatter, Brandeis, & Strik, 1997) and it points toan inhibitory function tapped by this component. Wealso observed longer P3 latencies on no-go than go trials.Often, higher-amplitude components are also quickerto appear, but Eimer (1993) reported longer latency

P3s on no-go trials as well. This pattern of results (great-er amplitude, longer latency) seems consistent withFalkenstein et al.’s (1999) suggestion that the inhibitoryP3 marks the closing of an inhibitory window. Finally, P3amplitudes decreased with age on no-go trials only.Amplitudes remained low and did not change develop-mentally for go trials. This finding seems particularlyinteresting because it integrates the functionality ofthe frontal P3 with a developmental trend suggestingincreased efficiency with age. Whether or not the frontalP3 taps the termination of an inhibitory process, its rolein response inhibition appears to require less corticalactivation as children mature.

Source modeling suggested a steady developmentaldecline in the activation of a mid- or posterior cingulatesource underlying the N2, roughly paralleled by a de-velopmental increase in the activation of an anteriorcingulate source. These results point to a process offrontalization as children mature, consistent with otherresearch (e.g., Bunge et al., 2002; Rubia et al., 2000). AnACC generator for the N2 has frequently been reportedfor adults (e.g., Nieuwenhuis et al., 2003; Tucker, Luu,Desmond, et al., 2003; van Veen & Carter, 2002). How-ever, our results suggest that it is not until middlechildhood or early adolescence that ACC activity isevident, consistent with Bunge et al.’s (2002) descrip-tion of immature prefrontal activation in children. Anadditional source was identified for the two older agegroups in the emotion-induction block only, in rightinferior frontal or temporal cortex, suggestive of poste-rior OFC or temporal pole activity. Ventral prefrontalregions have been associated with the processing ofnegative emotion (Drevets & Raichle, 1998) or emotionregulation (Davidson, Putnam, & Larson, 2000), and theright OFC has been specifically linked to responseinhibition (Cunningham, Raye, & Johnson, 2004). Tem-poral pole activation has been associated with the in-duction or reactivation of negative emotions such asanxiety and anger in children as well as in adults (e.g.,Nelson et al., 2003; Kimbrell et al., 1999). Thus, in thepresence of negative emotion, children in middle child-hood and adolescence may have applied ventrally me-diated inhibitory controls independent of the deliberateself-monitoring that is generally associated with dorsalprefrontal activities. Finally, it is interesting to note thatthe oldest two age groups demonstrated more imma-ture source solutions in Block B relative to Block A: thetransition to Block B activated the more posteriormidline source for the oldest children and deactivateda small anterior midline source for the 9–12-year-olds.Although merely suggestive, these results imply that re-sponse inhibition in the presence of negative emotionrecruits cortical activities that are less sophisticated orless developed.

In conclusion, the results of this research indicate adecline in ERP amplitudes and latencies with age fortwo ERP components tapping inhibitory control. In

Lewis et al. 441

combination with these findings, increased dorsomedialfrontal activation with age suggests that cortical activitiesmediating inhibitory control become both more local-ized to prefrontal structures and more limited in overallactivation. Superimposed on this developmental trend,negative emotion induction produced higher ERP am-plitudes specific to response inhibition, with an indica-tion of right ventral activation in middle childhoodthrough adolescence. This pattern of results indicatesthat inhibitory processes recruited for emotion regula-tion involve differing cortical regions as children mature.

Acknowledgments

We gratefully acknowledge the financial support provided bygrant No. 1 R21 MH67357-01 from the Developmental Psycho-pathology and Prevention Research branch of the National In-stitute of Mental Health (NIMH), as well as support from theCanadian Institutes for Health Research (CIHR) and the Nat-ural Sciences and Engineering Research Council of Canada(NSERC). We are also grateful for support provided (to PDZ)by the Canadian Foundation for Innovation.

Reprint requests should be sent to Marc D. Lewis, Departmentof Human Development and Applied Psychology, OntarioInstitute for Studies in Education, University of Toronto, 252Bloor Street West, Toronto, Ontario M5S 1V6, Canada, or viae-mail: mlewis@oise.utoronto.ca.

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